Background: Angiogenesis has been demonstrated in acute cerebral infarct lesion. Intracranial atherosclerotic stenosis(ICAS)is usually associated with chronic cerebral ischemia. It is uncertain whether angiogenesis exist in such circumstance. αvβ3-integrin is expressed by angiogenic endothelial cells and serve as a biomarker of angiogenesis. 68Ga-PRGD2 which is a PET tracer specifically binding to toαvβ3-integrin was used for imaging angiogenesis. Objective: To evaluate the status of angiogenesis in patients with severe ICAS. Method: For the pilot study, patients with unilateral ICAS were recruited. 68Ga-PRGD2 PET/CT, 13N-Amonia PET/CT and 18F-FDG PET/CT scans were performed. The procedures were done at least 45 days after index ischemic event in symptomatic ICAS patients. The PET images were evaluated by semi-quantitative analysis. Peak standardized uptake value (pSUV)were calculated. pSUV was compared between hemisphere supplied by ICAS and opposite side. Correlation analysis were applied between pSUV of 68Ga-PRGD2, and 13N-Amonia. Informed consent were obtained. Results: Nine patients were studied, 6 with symptomatic (45 days to 19 years post ischemic event) and 3 asymptomatic ICAS. Among them, there were 3 ICA occlusion, 3 MCA occlusion and 3 MCA stenosis (unilateral ≥70%). 68Ga-PRGD PET/CT showed significantly higher pSUV in lesion sides (0.22 vs 0.08, P<0.02 ). There are no significant difference between SUV of 13N-Amonia (3.59 vs 3.90,p=0.489) and 18F-FDG(12.42 vs 13.86,p=0.34). pSUV of 13N-Amonia in lesion sides significantly correlates with pSUV of 68Ga-PRGD2 (r=-0.77, P=0.015). Conclusion: 68Ga -PRGD2 uptake was observed beyond acute phase in patient with severe ICAS. Chronic cerebral ischemic might induce angiogenesis in addition to acute ischemic event. Further study to explore the mechanism was warranted. Fig.1 Images of a TIA patient 45 days after onset. C. Obvious uptake of 68Ga -PRGD2 (arrow). D. Lightly low uptake of 18F-FDG .